Researchers Discover Protein that Triggers Islet Cell Rejection

This press release is an announcement submitted by The Journal of Clinical Investigation, and was not written by Diabetes Health.

A new system based on the islet rejection mechanism has been shown to vastly increase transplant efficiency

Feb 9, 2010

Researchers at RIKEN and Fukuoka University have pinpointed the mechanism responsible for early rejection of transplanted pancreatic islet cells in the treatment of type 1 diabetes. A new system based on this mechanism has been shown to vastly increase transplant efficiency, setting the stage for the development of powerful new treatment techniques.

 Currently, the most widely used treatment for type 1 diabetes is the regular injection of insulin, a burdensome task for patients. Islet cell transplantation, whereby insulin-producing cells from a donor pancreas are transplanted into the patient's liver, is a promising alternative approach. However, it has achieved limited success due to a strong and rapid immune-mediated rejection of the transplanted islets.

With their discovery, the researchers have demonstrated that HMGB1 (high-mobility group box 1), a nuclear protein whose precise function has heretofore remained elusive, is in fact produced by the islet cells and directly triggers their early rejection. Based on this finding, they developed a system to measure the level of HMGB1 in the blood and determine the onset of rejection, information which they used to establish a treatment four times more effective than earlier islet transplantation protocols.

While shedding light on a previously unknown function of a major nuclear protein, the discovery of the HMGB1-mediated pathway also represents a breakthrough in diabetes research. For millions of diabetes sufferers around the world, its application to islet transplantation promises great improvements in this technique, bringing dreams of insulin independence one step closer to reality.

This paper is published in the February issue of The Journal of Clinical Investigation. Please click here to read the paper.

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Source:

The Journal of Clinical Investigation press release

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Categories: Beta Cells, Diabetes, Diabetes, Insulin, Islet & Pancreas Transplant, Research, Type 1 Issues


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Comments

Posted by Anonymous on 9 February 2010

Wonderful news! Another step closer.

Posted by Anonymous on 9 February 2010

Ask BMS, they made a antibiotic that caused diabetes...bet they have the ablity to help but like their antibiotic as they stated over and over again...It's not profitable!

Posted by Anonymous on 9 February 2010

I would love to consider transplantation as an option for treatment. The risk of rejection as well as the side effects of the anti-rejection medication has kept me from following through with applying. It would be amazing if researchers could make this a safer and effective procedure. No one likes taking 3-5 shots a day or having an insulin pump attached to them all the time! Oh, to return to normal life!

Posted by Anonymous on 10 February 2010

Could this be used in conjunction with Dr. Faustman's work with TNF alpha? First kill the actively rogue T-cells that attack islets with BCG (TNF alpha), then use this protein to induce tolerance so that there is no longer an autoimmune response. We already know through numerous studies that islet regeneration is a continuous process but is negated by the underlying autoimmunity. Could this be the missing link? The breakthrough that with Dr. Faustman's work, could lead to, finally, a real cure for Type 1 Autoimmune Diabetes? I'm cautiously optimistic.

Once researchers found and isolated the peanut protein, they used it to induce tolerance. http://www.cbsnews.com/video/watch/?id=4867787n

Posted by Anonymous on 10 February 2010

Finally, Some Hope :)


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